Hepatitis C virus (HCV) has tropism for other tissues besides the liver (e.g. lymphocytic tissues). It has been isolated from the myocardium of patients with myocarditis and cardiomyopathy hence, its inclusion among the cardiotropic viruses; however, the mechanisms by which this virus damages the myocardium have not been elucidated. It seems that the development of HCV-associated cardiomyopathy may take place in genetically susceptible individuals in whom viral, immunologic, and apotoptic mechanisms may act in concert to produce myocardial damage. In this regard, the HLA and non-HLA systems have been implicated in the susceptibility for the development of HCV-associated cardiomyopathy. In this article, possible mechanisms by which the HCV may cause cardiomyopathy are proposed based on recent knowledge on the behavior of this virus, and on current ideas on the pathogenesis of cardiomyopathy. The understanding of cardiomyopathy as an extrahepatic manifestation of HCV infection is of great importance because the treatments available for chronic hepatitis C at present are considered relative contraindications in patients with myocardial dysfunction. However, if causative and pathophysiologic mechanisms underlying HCV-associated cardiomyopathy are further elucidated patients with chronic hepatitis C and non ischemic cardiomyopathy may benefit from therapeutic interventions that may result in eradication of the virus and reversal of myocardial dysfunction.